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Diabetes Type I (Insulin Dependent Diabetes Mellitus, IDDM): It is cased due to deficient insulin production by pancreas because either beta cells of islets of Langerhans are not able to produce insulin or beta cells are absent. It is kept under control by administration of insulin in case of insulin dependent diabetes. Science, Technology and Medicine open access publisher.Publish, read and share novel research. NicoluaJC, Maia LN, vitola JV, Mahaffey KW, Machado MN, Ramires JA, Baseline glucosa and left ventricular remodeling after acute myocardial infarction. Diabetes is the No.1 cause of blindness kidney failure amputations and nerve disease in the United States. I would highly central diabetes insipidus treatment guidelines recommend this journal for anyone who has Diabeties. Intensive glycemic control and an aggressive targeted multifactorial therapy for type 2 diabetes and its complications is the current standard of care Objec Pathophysiolo Review pathophysiology of Diabetes Mellitus. American Diabetes Association Diet dietary recommendations for type 1 and type 2 diabetes mellitus.
If the pancreas in a pregnant woman cannot keep up with the insulin needs the blood glucose levels will rise above desired levels.
Download Fast Foods For Diabetics To Eat from our sponsored partner fastest speed with unlimited downloads. The responses you have given us indicate thatyou do not have any risk factors for diabetes at this time. The liquid he mentioned was also diluted since one drop of pure LSD would be thousands of doses and the total amount of liquid in the eye-dropper quite valuable. DOCUMENTATION Of GLOBAL NANOTECHNOLOGY PROGRAM – Men foods to eat if you have type 2 diabetes Behind Chemtrails. Here are some limitations with using GI for food selection Many doctors are happy to medicate up when cutting carbs will likely mean no medication and will prevent one day needing insulin shots that can easily lead to weight gain. The announcement from Heel allows people who wouldn’t otherwise seek homeopathic treatment to feel more confident of its efficacy. Simply put: It’s like a party that you host and all of your friends attend and it turns out to be THE party of the year.
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I wonder if Dave Sharp and Dave Wood would agree with him on his analogy of beginning a start up business. One of my personal favorites is Rejection #30: Slide down the fire pole at a fire station. Your challenge, should you choose to accept it………………make sure that you document your progress through the 100 days. Cushing’s disease is a serious condition of an excess of the steroid hormone cortisol in the blood level caused by a pituitary tumor secreting adrenocorticotropic hormone (ACTH). Cushing’s disease is rare, affecting 10 to 15 people per million each year, most commonly adults between 20 and 50 years of age. Mood and behavior disorders; some patients have psychiatric disorders that require hospitalization. The early stages of Cushing’s disease may be difficult to recognize, especially because the body changes develop slowly. The diagnosis may be difficult to make because sometimes the hormone elevations come and go: so called “cyclic” or “periodic” Cushing’s disease. Your doctor will conduct a thorough physical exam and ask you about your symptoms and medical history. Since I’ve been down the “Cushie” road before, and had my first pituitary surgery May 2006 at UCSF, I’ve personally gone through many of the signs, symptoms, diagnostic tests, and seen way to many drs. If you’ve got a story to tell, you can do what so many others and I are doing, write about it.
Much of the information found in this post was taken from UCLA Health Systems Pituitary Tumor Program page. What is really cool is the fact that if I wake up with an idea or had a good dream, I have a place I can go to and be productive.
What better cause is there than to share this really awesome company, Empower Network, and their blogging platform that even a 12 yr. It results in deficient passage of glucose form blood into the cell surfaces for storage or for direct consumption. ADH is released into blood when special osmoreceptors  or hypothalamic neurons are stimulated by rise in osmotic pressure of blood due to loss of water from the body. Potential mechanism by which hyperglycemia-induced mitochondrial superoxide overproduction activates four pathways of hyperglycemic damage. In the absence of acute hyperglycemia, prodromal angina was associated with preserved predischarge in left ventricular ejection fraction (LVEF). Importance of glucose levels in diabetic and nondiabetic patients in acute myocardial infarction.
Changes in myocardial perfusion indexes after overnight fasting (baseline) and 120 minutes after standard mixed meal ingestion (postprandial) in type 2 diabetic patients (blue bars) and control subjects (red bars). Lopez Hernandez[1] Internal Medicine Division, Ecatepec General Hospital, Mexico State Health Institute,, Mexico1.
The most common causes are underlying infection disruption of insulin treatment and new onset of diabetes.
Most people who develop type 2 diabetes are obese.49 More precisely people with excess abdominal fat (as opposed to fat Effects of two high-fat diets with different fatty acid Difference Between Type1 And Type 2 Diabetes Chart compositions on glucose and lipid metabolism in healthy young women. Just diabetes prevention and management workshop 2014 heard boiling ocra then drinking the water cures diabetes. Not sure if trolling but… Stopping the US and crippling its capacities at this moment in time is better than it functioning at all. The American Diabetes Association is leading the fight to Stop Diabetes and its deadly consquences and fighting for those affected by diabetes. In an early stage clinical trial of 11 people funded by Diabetes UK all reversed their diabetes by drastically cutting their food intake to just 600 calories a day for Patients or GPs who would like more information about the diet that reverses Type 2 diabetes see the Magnetic Resonance Centre website.
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RebelMouse is solving a core problem of how to highlight community and bring together disparate social efforts across all the important networks. However, it can be difficult to diagnosis Cushing’s disease, and the diagnosis is often delayed. Comparing old and recent photographs often shows the changes in facial appearance and physical characteristics of the body. Glucocorticoids are also used to suppress the immune system after transplantation to keep the body from rejecting the new organ or tissue. It may occur due to defective insulin receptors over cell surfaces or abnormality on plasma protein amylin.
Excess superoxide partially inhibits the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), thereby diverting upstream metabolites from glycolysis into pathways of glucose overutilization. Among patients with acute hyperglycemia, there was no significant difference in predischarge LVEF between patients with (blue bars) and without prodromal angina (red bars). It is near-linear in patients without diabetes (blue) but U-shaped in patients with diabetes (red).


IntroductionThe proposal of this chapter is explain the importance and relevance of the understanding of the role that play the level in the serum glucose during the acute myocardial infarction (AMI). Difference Between Type1 And Type 2 Diabetes Chart there are many ways to manage type 2 diabetes. Lack of glucose energy to the brain can cause symptoms ranging from headache mild confusionabnormal behavior loss of consciousness seizure and coma. Description: The Microalbumin urine test for kidney function i often used as a screening to evaluate the risk for kidney failure for people with chronic common signs of diabetes type 2 conditions like diabetes or hypertension. Compare halth insurance Difference Between Type1 And Type 2 Diabetes Chart borderline diabetes management online.
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ACTH stimulates the adrenal glands (located on top of the kidneys) to produce cortisol, commonly referred to as the stress hormone. This results in increased flux of dihydroxyacetone phosphate (DHAP) to diacylglycerol (DAG), an activator of protein kinase C (PKC), and of triose phosphates to methylglyoxal, the main intracellular AGE precursor. Adapted from Ishihara et al Ischemic preconditioning delays infarct progression during the early hours after the onset of AMI and extends the window of time for reperfusion therapy[43]Table 1. Since many years the investigation in this area has showed that the hyperglycemia is a strong predictor of mortality in acute myocardial infarction, as representation of the response of the myocardial cell to the ischemic injury, related mainly to acute catecholamine release.Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in individuals with diabetes, for which 65% of deaths are attributable to heart disease or stroke. Inoue, Impact of admission hyperglycemia and diabetes mellitus in short and long term mortality after acute myocardial infarction in the coronary intervention era.
Uncontrolled gestational diabetes also increases the risk of jaundice and breathing problems in the newborn. Increased flux of fructose-6-phosphate (Fructose-6-P) to UDP-N-acetylglucosamine increases modification of proteins by O-linked N-acetylglucosamine(GIcNAc), and increased glucose flux through the polyol pathway consumes NADPH and depletes glutathione. The effect of hyperglycemia and diabetes in outcomes for thrombolysis, arrhythmias and left ventricle function7.
James, et al.Unrecognized glycometabolic disturbance as measured by hemoglobin A1c is associated with a poor outcome after acute myocardial infarction. In the results in a re analysis of HEART2D study results, the intraday glucose variability as target compared with the basal glucose, in diabetic type 2 patients after myocardial infarction, showed similar overall glycemic control but did not result in a reduction in cardiovascular outcomes[4]. Gestational diabetes s high blood sugar that develops at any time during pregnancy in a woman who does not have diabetes.
Treating diabetic survivors of AMI with prandial versus basal strategies achieved differences in fasting blood glucose, less-than-expected differences in postprandial blood glucose, similar levels of A1C, and no difference in risk for future cardiovascular event.2. Stroke, Subcommittee, Hyperglycemia and Diabetes in Myocardial Infarctionstics Committee and Stroke Statistics Subcommittee.
Diabetes mellitus and risk for myocardial infarctionThe main cause of death in the industrialized countries is the coronary artery disease (CAD). In United States, diabetes is the most prevalent risk factor for cardiovascular events[5] The patient with diabetes mellitus have increased risk for cardiovascular disease, a risk that contributes to a significant decrease in life expectancy.
Cox, Is blood glucose an independent predictor of mortality in acute myocardial infarction in the thrombolytic era? The patients with diabetes have a risk for myocardial infarction (MI) comparable to that of the risk of recurrent myocardial infarction in a patient without diabetes. In patients with acute myocardial infarction the underlying mechanism in the increase of mortality associated to glucose levels are poor understood. In a study by Nicolau JC and cols, with 52 patients with acute myocardial infarction with ST segment elevation and hyperglycemia, in the first 24 hours compared radionuclide ventriculography at day 4 and six months, finding that basal glucose level like independent and powerful predictor of left ventricular growth after an acute myocardial infarction[10]Hyperglycemia increases the morbility and mortality in hospitalized patients in Intensive Care Units with acute myocardial infarction, stroke and those with aortocoronary bypass. Verges, Prevalence and impact of metabolic syndrome on hospital outcomes in acute myocardial nfarction. The treatment with infusion of insulin has showed a better outcome in these patients[11]A1c hemoglobin (A1cHb) or glycosilated hemoglobin is a marker of the glucose level in two previous months, and that is affected in minimal mode by the levels of glucose associated to acute coronary syndromes. In the OPTIMAAL study, in Danish population with acute myocardial infarction complicated with heart failure, was concluded that A1cHb levels showed to be a predictor of mortality in patients without diabetes previously known.[12]In a Japanese study was evaluated the impact of elevated level of glucose in patients with acute myocardial infarction with percutaneous coronary intervention, concluding that the hyperglycemia at time of admission was associated with a increased mortality a short term (30 days), and that the presence de diabetes mellitus was associated a poor outcome at long term (3 years), considering that both, the acute hyperglycemia in myocardial infarction and diabetes mellitus must be treated as two different problems[13]3.
Mechanisms induced by hyperglycemia than increased risk in acute myocardial infarctionAcute phase hyperglycaemia and diabetes are both associated with adverse outcomes in acute myocardial infarction, with higher reported incidences of congestive heart failure, cardiogenic shock, and death.
However, the association between hyperglycaemia and adverse outcomes is not confined to patients with diabetes.
The mechanism is not clear, but it is commonly regarded as a response to stress resulting from catecholamine induced glycogenolysis. Insulin resistanceInsulin resistance is a hallmark in diabetes mellitus type 2 and obesity, the resistance to action of insulin in skeletal muscle, leads to a decrease in the glucose disposal and the use of fatty acids and compensatory hyperinsulinemia.[14] With relative insulinopenia, however, the ischemic myocardium is forced to use free fatty acids instead of glucose as an energy source because myocardial glucose uptake is acutely impaired.
Thus, a metabolic crisis may ensue as the hypoxic myocardium becomes less energy efficient in the setting of hyperglycemia and insulin resistance.The SMART study group published a prospective cohort study in 2611 patients with manifest arterial disease without known diabetes.
The relation of HOMA-IR with cardiovascular events (vascular death, myocardial infarction or stroke) and all causes of mortality were assessed. In patients with manifest arterial disease without known diabetes, the results of this trials concludes than insulin resistance increases with the number of metabolic syndrome components, and elevated insulin resistance increases the risk of new cardiovascular events[15]Diabetes mellitus type 2 is result of two developments, a chronic overnutrition with resultant insulin resistance and least a relative failure of pancreatic ?-cells to release sufficient insulin to maintain glucose homeostasis.
Commonly, attempts are made using the homeostasis model of insulin resistance[16]Intact pro insulin is a precursor molecule of the insulin that is released into circulation.
Proinsulin is associated with increased resistance to insulin, and have a similar adipogenetic activity than insulin, but only the 10% to 20% of the glucose-lowering effect. Recently, determination of proinsulin has been used as a diagnostic tool because an increasing proinsulin to insulin ratio predicts insulin resistance and deterioration of glucose tolerance.[17] Hyperglycemia is a reflection of relative insulinopenia, which is associated with increased lipolysis and free fatty acid generation, as well as diminished myocardial glucose uptake and a decrease in glycolytic substrate for myocardial energy needs in STEMI. Endothelial dysfunctionA single layer of endothelial cells lines the inner surface of all blood vessels, providing a metabolically active interface between blood and tissue that modulates blood flow, nutrient delivery, coagulation and thrombosis, and leukocyte diapedesis. It synthesizes important bioactive substances, including nitric oxide and other reactive oxygen species, prostaglandins, endothelin, and angiotensin II, that regulate blood vessel function and structure. Nitric oxide potently dilates vessels and mediates much of the endothelium’s control of vascular relaxation. A number of fundamental mechanisms contribute to the decreased bioavailability of endothelium-derived nitric oxide in diabetes:Hyperglycemia inhibits production of nitric oxide by blocking eNOS synthase activation and increasing the production of reactive oxygen species, especially superoxide anion (O2?), in endothelial and vascular smooth muscle cells. Williams et al assessed endothelium-dependent vasodilation through brachial artery infusion of methacholine chloride in non-diabetic subjects. DyslipidemiaCharacteristic abnormalities in the lipid profile in type 2 diabetes include elevated triglyceride levels, decreased atheroprotective high-density lipoprotein (HDL) levels, and increased levels of small dense LDL. Cholesteryl ester concentrations may regulate VLDL production, with increased concentrations resulting in elevated VLDL synthesis.
Overproduction of triglyceride-rich lipoproteins and impaired clearance by lipoprotein lipase lead to the hypertriglyceridemia common in diabetes. Elevated levels of triglyceride rich lipoproteins lower HDL levels by promoting exchanges of cholesterol from HDL to VLDL via cholesteryl ester transfer protein.
Diabetic patients with CAD more commonly have the combination of elevated triglycerides and low HDL than elevated total and LDL cholesterol levels.Strongly related to insulin resistance, obesity is a known risk factor for heart failure. InflammationIn a study Esposito et al[26] measured circulating levels of cytokines, including interleukin (IL)-6, IL- 18 and tumor necrosis factor-? in subjects with normal or IGT during 3 consecutive pulses of intravenous glucose separated by a 2-h interval. The plasma cytokine levels increased as the blood glucose level increased but immediately returned to normal as glucose returned to normal levels. Interestingly, when the first elevation in the blood glucose level was maintained by subsequent continuous intravenous glucose infusion, plasma cytokine concentrations gradually returned to normal levels.The exact mechanism by which glucose stimulatespro inflammatory events is not clear, although indirect evidence suggests that it does so possibly by stimulating production of tumor necrosis factor (TNF)-? (a pro inflammatory cytokine). A diet with a high glycemic load and hyperglycemia induced production of acute-phase reactants. Similar to glucose, TNF-? also enhances free radical generation by augmenting polymorphonuclear leukocyte NADPH oxidase activity, activates NF-?B, and increases intercellular adhesion molecule-1 expression in endothelial cells. This similarity in the actions of glucose and TNF-?, and the ability of former to enhance acute phase reactants suggests, but does not prove, that glucose may enhance TNF-? production and brings about its pro inflammatory actions.TNF-? is secreted by adipose tissue, macrophages and cardiac tissue, and plays roles in the pathogeneses of insulin resistance, type 2 diabetes mellitus, inflammation, and septic shock. It has been reported that hyperglycemia elevates coagulant activation markers, including thrombin antithrombin complexes and soluble tissue factor, whereas hyperinsulinemia inhibits fibrinolysis.Platelets can modulate vascular function and participate significantly in thrombus formation. Abnormalities in platelet function may exacerbate the progression of atherosclerosis and the consequences of plaque rupture. Intraplatelet glucose concentration mirrors the extracellular concentration, since glucose entry into the platelet does not depend on insulin.
These abnormalities may result from decreased endothelial production of the anti aggregants nitric oxide and prostacyclin, increased production of fibrinogen, and increased production of platelet activators, such as thrombin and von Willebrand factor.
Thus, diabetic abnormalities increase intrinsic platelet activation and decrease endogenous inhibitors of platelet activity 3.6.


PAI-1 inhibits the conversion of plasminogen into plasmin and consequently reduces fibrinolytic activity. An in vivo study in healthy volunteers using a hyperinsulinemic euglycemic clamp, demonstrated a 2.5-fold increase in levels of PAI-1 relative to baseline. This study suggested that impaired fibrinolysis in patients with diabetes is mediated by hyperinsulinemia rather than hyperglycemia.[33]Hyperinsulinemia increases PAI-1 levels by stabilization of the PAI-1 messenger RNA transcript through the actions of insulin and insulin-like growth factor type 1. Adipocytes have been found to be a major source of PAI-1, providing a direct link between obesity and a suppressed fibrinolytic system. Finally, inflammatory cytokines such as transforming growth factor-beta and tumor necrosis factor-alpha both of which are believed to have important roles in the metabolic syndrome increase the release of PAI-1 from adipose tissue4.
The hyperglycemic effect in the outcomes in acute coronary syndromesAcute hyperglycemia is associated with multiple biological effects that contribute to a poor outcome of the acute coronary syndromes, [34] this effects are listed in the table number 1 Admission hyperglycemia is associated with long-term risk for ACS mortality[35],but this association is not homogeneous in different ACS presentations,[36] unstable angina, NSTEMI, or STEMI.
Ischemic preconditioning is a potent endogenous cardioprotective mechanism that is promoted by the brief transient ischemia proceeding subsequent prolonged ischemia and reperfusion. Many studies have shown that an elevated plasma glucose level on admission is a major independent predictor of in-hospital and long-term outcome in patients with acute myocardial infarction, regardless of diabetes status.Acute hyperglycemia is common in patients with STEMI even in the absence of a history of diabetes. Hyperglycemia is encountered in up to 50% of all STEMI patients, whereas previously diagnosed diabetes mellitus is present in only 20% to 25% of STEMI patients.
The prevalence of type 2 diabetes mellitus or impaired glucose tolerance may be as high as 65% in myocardial infarction patients without prior diabetes when oral glucose tolerance testing is performed. High blood glucose concentration may increase risk of death and poor outcome after acute myocardial infarction.
Capes SE et al did a systematic review and meta-analysis to assess the risk of in-hospital mortality or congestive heart failure after myocardial infarction in patients with and without diabetes who had stress hyperglycemia on admission. There is a linear correlation between the blood glucose level on admission and mortality after acute myocardial infarction. Therefore, there is no clear cut-off value of blood glucose to predict mortality and no consensus about the appropriate definition of acute hyperglycemia for patients with myocardial infarction. Diabetes has been a consistently powerful risk factor for development of post infarction heart failure, accounting for 66% of mortality during the first year.
The combination of diabetes and HF after MI requires preventive action because it is usually not associated with the characteristic left ventricular remodeling. If left ventricular remodeling does develop, it requires appropriate treatment that includes revascularization and metabolically and hemodynamically effective treatment strategies that limit infarct size, cardiac dysfunction, and left ventricle remodelingIn patients without a history of diabetes, there was a linear relation between admission blood glucose level and in-hospital mortality (Figure 5)Figure 5.Relationship between admission blood glucose level and in-hospital mortality. A cell surface receptor for this glycated end products (a “RAGE”) has been isolated; binding of AGEs and other pro inflammatory ligands to this signal-transducing receptor has a multitude of effects, including increased smooth muscle cell proliferation, migration and activation of mononuclear phagocytes, induction of cytokines such as TNF-?, and in endothelial cells, increased vascular permeability, oxidative stress, vasoconstriction and expression of adhesion molecules.
Glucotoxic effects involve three additional mechanisms for dysfunction in the diabetic heart. The effect of hyperglycemia and diabetes in outcomes for thrombolysis, arrhythmias and left ventricle functionIn patients with acute STEMI, thrombolysis in myocardial infarction (TIMI) frame counts may show significant variability despite presence of grade 3 TIMI flow after successful reperfusion and lower TIMI frame counts after reperfusion are associated with more favorable prognosis. No data are present regarding TIMI frame counts and admission glucose values in non-diabetic patients with acute ST elevation MI who undergo successful primary percutaneous coronary intervention. This increased risk of complications is one of the possible explanations for the elevated in-hospital mortality in AMI patients presenting with hyperglycemia. The patients were implanted with an implantable loop recorder and followed for 2 years allowing continuous monitoring and diagnosis of asymptomatic and symptomatic arrhythmias.[57] Diastolic dysfunction in post myocardium infarcted patients with moderate-to-severe left ventricle systolic dysfunction predisposes to cardiovascular ischemic events such as re-infarction and stroke.
New-onset atrial fibrillation also occurs more frequently in patients with diastolic dysfunction.
Re-infarction and stroke were more frequent in patients with new onset atrial fibrillation, but the increased risk of ischemic events was independent of development of atrial fibrillation, suggesting that diastolic dysfunction in infarcted patients by itself is an important risk factor for ischemic events.[58]Diabetes is associated with a higher risk of death or heart failure hospitalization across the spectrum of left ventricle ejected fraction (LVEF) in high-risk post-myocardial infarction patients. The magnitude of reduction in risk of death or heart failure hospitalization associated with increasing LVEF is significantly attenuated among patients with diabetes when compared to patients without diabetes[59]VALIANT was a randomized, double-blind trial of the efficacy and safety of Valsartan versus Captopril versus combination therapy following MI complicated by clinical or radiological signs of heart failure, evidence of left ventricle systolic dysfunction (LVEF ? 35% by echocardiography or ?40% by radionuclide ventriculography), or both[60]7. Glucose variability in acute myocardial infarctionHyperglycemia is a strong predictor of mortality in patients hospitalized with acute myocardial infarction. Professional society guidelines have accordingly advised glucose control in hyperglycemic patients. These same guidelines also recommend avoiding hypoglycemia, even though the association between hypoglycemia and adverse outcomes in acute myocardial infarction patients is controversial. In contrast, only hypoglycemia on admission predicted death, and this relationship dissipated after admission. These data suggest hypoglycemia may not be a direct mediator of adverse outcomes in myocardial infarction[61]Short-term variation in blood glucose levels is a daily challenge for patients with diabetes. It confers a possible increased risk for hypoglycemia, and it has been suggested that glucose variability is related to cardiovascular risk [62]–[64].
In diabetic patients without microvascular or macrovascular complications, postprandial myocardial perfusion defects may represent an early marker of the atherogenic process in the coronary circulation; hence, its reversal constitutes a potential goal of treatment[66]. For example, the United Kingdom Prospective Diabetes Study Group (UKPDS) study found that “intensive” control of fasting blood glucose among diabetic patients reduced the relative risk for myocardial infarction by only 16% as compared to conventional, diet-based therapy (p=0.052).[67] What, then, accounts for the greatly increased cardiovascular risk among patients with diabetes? Postprandial hyperglycemia, which captures “spikes” in blood glucose levels that may not be fully reflected in fasting blood glucose or glycosylated hemoglobin levels[67], has historically been overlooked as a CV risk factor among diabetic patients, those with isolated impaired glucose tolerance and those in the general population.8. However, there is broad epidemiological evidence that just as acute hyperglycemia portends a poorer clinical outcome among critically ill patients, postprandial hyperglycemia predicts cardiovascular disease and mortality not only among patients already identified as diabetic, but also among subjects in the general population. Mounting mechanistic evidence suggests that acute hyperglycemia has myriad adverse effects that are mediated through oxidative stress.
Moreover, some available interventional studies suggest that strategies directed toward decreasing postprandial glucose in outpatients and acute hyperglycemia during hospitalizations for cardiovascular events may improve clinical outcomes.
Postprandial hyperglycemia determines myocardial perfusion defects in type 2 diabetic patients. The 90-day mortality was significantly higher in the intensive control group than in the conventional-control group (27.5%vs. After these studies, recent guidelines revised their recommendation from intensive glucose control to mild glucose control, avoiding hypoglycemia.Due as an emerging risk factor for cardiovascular disease, acute hyperglycemia during cardiovascular events may be considered analogous to postprandial hyperglycemia and may carry with it similar adverse clinical implications. Accordingly, several groups, including the American Diabetes Association[71] and the American Heart Association[72], have encouraged more rigorous control of blood glucose levels during acute hospitalizations for cardiovascular diseases. The clinical trial basis for these recommendations is not yet exceedingly robust.Although sustained chronic hyperglycemia produces excessive protein glycation, acute fluctuations of glucose may activate oxidative stress and contribute to endothelial dysfunction, which may also participate in the development of diabetes complications.
Therefore, reducing postprandial hyperglycemia and glucose variability are now recognized as a priority in treatment of type 2 diabetes.
Therapeutic agents acting on postprandial glucose excursions are of particular interest to diminish glucose variability. Emerging therapeutic agents such as the glucagon-like peptide 1 agonists and the dipeptidyl peptidase (DPP)-4 inhibitors are very attractive.
Both increase insulin secretion and suppress glucagon release in response to meals, in a glucose-dependent manner.
This review will focus on the increasing impact of postprandial hyperglycemia and glycemic variability in developing diabetes complications and the role of DPP-4 inhibitors (sitagliptin, vildagliptin, saxagliptin) in reducing both defects presenting in people with type 2 diabetes.[74]In the more recent DIGAMI-2 study (n= 1253 patients), however, mortality did not differ significantly between diabetic patients randomized to either acute insulin infusion followed by insulin-based long-term glucose control, insulin infusion followed by standard glucose control, or standard management, probably reflecting a lack of difference in glucose control among the three groups[75]Because hyperglycemia remained one of the most important predictors of outcome in acute coronary syndromes, however, it appears to be reasonable to keep glucose levels within normal ranges in diabetic patients.
There was no difference in mortality rates among the groups during hospitalization or at 3 or 6 months. Conclusions and recommendationsConcluding, there is currently insufficient evidence to consider glucose control as a quality measure during acute myocardial infarction hospitalization, although this position may change in the future.
Although efforts to optimize glucose control may also be considered in patients with milder degrees of hyperglycemia, the data regarding a benefit from this approach are not yet definitive, and regardless of diabetes status.
Insulin, administered as an intravenous infusion, is currently the most effective method of controlling glucose among patients hospitalized in the ICU. Effective protocols for insulin infusion and glucose monitoring have been developed in other patient populations. The evidence in clinical trials has showed the importance of admission glucose and glycated hemoglobin, in the evolution, risk for complications, and therapeutic response of patients with acute myocardial infarction.
The control of blood glucose levels in patients with acute myocardial infarction, will lead to better outcomes regardless of diabetes status.



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